Transient Gyral Enhancement After Epileptic Seizure in a Patient with CREST Syndrome

WOS: 000419248500012Limited scleroderma, also termed CREST syndrome (calcinosis cutis, Raynaud's phenomenon, esophageal dysmotility, sclerodactyly and telangiectasia), is a form of scleroderma which is an autoimmune connective tissue disease. Neurological involvement is less common than other system involvements in scleroderma. Epileptic seizure is a rare neurological complication. Gyral enhancement is not an expected finding during disease. Gyral enhancement is contrast enhancement of superficial brain parenchyma and it usually occurs as a result of vascular, inflammatory, infectious and neoplastic processes. A-sixty-seven-year old female patient, who was diagnosed as CREST syndrome for three years was admitted to our hospital. She had an epileptic seizure three days ago and behavioral changes after the seizure. There was not epilepsy diagnosis in her medical history. In neurological examination; she was apathic and deep tendon reflexes were hyperactive, Hoffman's and Babinski reflexes were positive on the right side of her body. In laboratory studies; anti-nuclear antibody was positive at 1/1000 and anti-centromere antibody was positive. On contrast-enhanced cranial magnetic resonance imaging (MRI); gyral enhancement was observed in the left parieto-occipital region. Cerebrospinal fluid tests were within normal limits. Electroencephalography demonstrated diffuse cerebral dysfunction. We administrated antiepileptic drug to the patient during hospitalization. On the follow up, apathy and restriction of the cooperation were improved. Epileptic seizure did not recur. After ten days, in the control cranial MRI, gyral enhancement was reduced significantly. Neurological involvement in CREST syndrome is rare and epileptic seizures have been appeared in a limited number in the literature. Inflammatory and vascular processes can cause gyral enhancement, but also it must be kept in mind that gyral enhancement can be observed transiently after epileptic seizure

Radial Nerve Neuropathies: A Retrospective Study

WOS: 000421133400007Objective: Radial nerve neuropathy is a rare neuropathy between upper extremity entrapment neuropathies developed because of various etiological factors. This study aimed to retrospectively evaluate patients referred to our EMG laboratory with a diagnosis of radial nerve neuropathy. Methods: In the study, the files of 41 patients who referred to our electromyography (EMG) laboratory with the radial nerve lesion diagnosis between 2004 and 2013 were retrospectively investigated. Results: Forty-one patients were included in this study. Of the patients, 36 were male (87.8%), five were female (12.2%), and the mean age was 42.36 +/- 15.21. Of the patients, 39% were referred by Orthopedics, 34.1% by Neurology, 24.4% by Physical Therapy and Rehabilitation, and 2.4% by Plastic and Reconstructive Surgery departments to our laboratory. Studying the relationship between the shape of nerve injury for etiological reasons shows that the humerus and radius fractures occur most frequently after falling. Conclusion: Therefore, the variety of etiological factors leading to the radial nerve lesions is remarkable. The higher incidence in male patients may be associated with more common factors such as trauma and work accidents in this gender. The electrophysiological examinations can provide valuable contributions to the diagnosis and follow-up of radial nerve neuropathy. On examining the EMG results of patients, the findings consistent with axonal lesion of radial nerve in the spiral grove after the triceps muscle were the most common (34.1%). The average recovery time of the patients could not be recorded because of the referred patients from other centers and the lack of control visits of the patients. It was found that five of the 10 patients contacted by phone had complete recovery, and there was no recovery in the other five patients

The COVID-19 from Neurological Overview

Elmali, Ayse Deniz/0000-0001-6380-9550; Afsar, Nazire/0000-0001-8123-8560; Sahin, Sevki/0000-0003-2016-9965;WOS: 000556540500002[No abstract available